Aging
Navigate
Submit an Article
Research Paper|Volume 12, Issue 23|pp 23822—23835

Calreticulin increases growth and progression of natural killer/T-cell lymphoma

Yan Zheng1, Chuntuan Li1, Pengliang Xin1, Qunyi Peng1, Weiyu Zhang2, Shengquan Liu1, Xiongpeng Zhu1
  • 1Department of Hematology, The First Hospital of Quanzhou Affiliated to Fujian Medical University, Quanzhou 362000, Fujian Province, China
  • 2Department of Pathology, The First Hospital of Quanzhou Affiliated to Fujian Medical University, Quanzhou 362000, Fujian Province, China
Received: June 22, 2020Accepted: July 25, 2020Published: November 18, 2020
https://doi.org/10.18632/aging.104030

Copyright: © 2020 Zheng et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

In this study, we investigated the role of calreticulin (CALR) in the pathogenesis of natural killer/T-cell lymphoma (NKTCL). CALR expression was significantly higher in the NKTCL tissues than normal control tissues in the GSE80632 dataset. High CALR expression correlated with poorer overall survival of NKTCL patients (P = 0.0248). CALR mRNA and protein levels were significantly higher in NKTCL cell lines (NK92, SNK6, and SNT8) than normal NK cells. CALR-silenced SNK6 cells generated significantly smaller xenograft tumors in immunodeficient NCG mice than control SNK6 cells. CALR-knockdown NKTCL cells showed significantly less in vitro proliferation and Transwell migration than the controls. CALR knockdown inhibited G1-to-S phase cell cycle progression by increasing the levels of p27 cell cycle inhibitor and reducing the levels of cyclin E2 and cyclin-dependent kinase 2 (CDK2). CALR knockdown inhibited epithelial-to-mesenchymal transition (EMT) by decreasing the levels of β-catenin and TCF/ZEB1 and upregulating E-cadherin. These data demonstrate that CALR regulates the growth and progression of NKTCL cells by modulating G1-to-S cell cycle progression and EMT.